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Neurobiol Dis. 2008 Oct;32(1):26-36. doi: 10.1016/j.nbd.2008.06.013. Epub 2008 Jul 3.

Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy.

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  • 1Davee Department of Neurology and Clinical Neurosciences, Feinberg School of Medicine, Northwest University Medical School, Chicago, IL 60611-3008, USA.


Many animal models of temporal lobe epilepsy (TLE) begin with status epilepticus (SE) followed by a latency period. Increased hippocampal pyramidal neuron excitability may contribute to seizures in TLE. I(h), mediated by h channels, regulates intrinsic membrane excitability by modulating synaptic integration and dampening dendritic calcium signaling. In a rat model of TLE, we found bidirectional changes in h channel function in CA1 pyramidal neurons. 1-2 d after SE, before onset of spontaneous seizures, physiological parameters dependent upon h channels were augmented and h channel subunit surface expression was increased. 28-30 d following SE, after onset of spontaneous seizures, h channel function in dendrites was reduced, coupled with diminished h channel subunit surface expression and relocalization of subunits from distal dendrites to soma. These results implicate h channel localization as a molecular mechanism influencing CA1 excitability in TLE.

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